Max Planck Institute for Dynamics and Self-Organization -- Department for Nonlinear Dynamics and Network Dynamics Group
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Genetic assimilation of visual cortical architecture

 

Although genetic information is critically important for brain development and structure, it is widely believed that neocortical functional architecture is largely shaped by activity dependent mechanisms. The information capacity of the genome, however, appears too small to contain a blueprint for hardwiring the cortex. Here we show theoretically that genetic mechanisms can circumvent this apparent information bottleneck.

PIC

Figure 1: Scheme of genetic networks specifying layout of orientation domains in V1. a) Shown is an example genetic subnetwork illustrating how morphogens regulate their expression rates mutually in neuronal nuclei. b) Morphogens are actively transported over dynamic long-range connections as indicated by the arrow. The transport of morphogens induces a signaling cascade, which exerts a regulation of morphogen expression. c) The concentration of morphogens in a neuron is illustrated by the colored dots. The difference of morphogen concentrations encodes orientation selectivity. d) Long-range connections are dynamic and target specific morphogen concentration profiles.
 

Using our prior reserach on universality classes of circuit self-organization in the visual cortex [1] , we devised mathematical models of genetic networks of neurons interacting by long-range axonal morphogen transport. Neurons dynamically generate morphogen patterns that prescribe the layout of orientation domains as experimentally observed in the primary visual cortex (V1) of primates and carnivores [2,3,4]. We use analytical methods from weakly non-linear analysis [5] complemented by numerical simulations to obtain solutions of example genetic networks. The hypothesis of genetic circuits shaping the complex architecture of V1 is in line with several recent biological findings. For instance, (1) transcription factors have been found to be transported via axons and to translocate into the nucleus of target neurons [6], (2) a molecular correlate was recently found for ocular dominance columns in V1 [7], (3) V1's architecture is intriguingly robust against radically abnormal developmental conditions such a dark rearing [8,2,4]. Our theory provides for the first time a scheme that shows how a complex cortical processing architecture can be specified using a genetic mechanism of small bandwidth.

[1]    F. Wolf, Phys. Rev. Lett. 95, 20 (2005)

[2]    M. Kaschube, et al., Science 330, 6007 (2010)

[3]    W. Keil, et al., Science 336, 6080 (2012)

[4]    M. Schottdorf, W. Keil, et al., PLoS CB 11, 11 (2015)

[5]    M. Cross, P. Hohenberg, Rev. of Mod. Phys. 65, 3 (1993)

[6]    S. Sugiyama, et al., Cell 134, 3 (2008)

[7]    K. Tomita, et al., Cerebral Cortex 23, 11 (2012)

[8]    L.E. White, et al., Nature 411, 6841 (2001)


Members working within this Project:

 Joscha Liedtke 
 Fred Wolf